The overall goal of this proposal is to identify the factors that are responsible for the decrease in cardiac output which occurs during cardiac tamponade and to determine their relative importance. The literature is contradictory concerning key aspects of the pathophysiology of both systolic and diastolic function during cardiac tamponade. A better understanding of this important clinical problem will lead to improvements in diagnosis in therapy. The role of myocardial contractility during cardiac tamponade has been controversial because a method of measuring contractility which was insensitive to the large changes in loading conditions which occur and a suitable conscious model of tamponade were not available. In our first study we will use a relatively load insensitive measure of left ventricular contractility, the end systolic pressure-volume relationship in our conscious canine model to test the hypothesis that myocardiac contractility is increased during cardiac tamponade and thus the striking decline which occurs in cardiac output is caused by impaired diastolic function. Left ventricular pressure (micromanometer) and volume (calculated from sonomicrometer measurements of three major axes) will be recorded as cardiac tamponade is induced by intrapericardial saline infusion (20 ml/min) to decompensation (DCT, 30% decrease in aortic blood pressure) as heart rate is controlled by atrail pacing (180 to 200 beats/min). The end systolic pressure - volume relationship produced by abrupt caval occlusion will be compared in slope to those inscribed during induction of tamponade and by sudden withdrawal of 20 to 30cc of pericardial fluid at DCT before and during beta adrenergic blockade. Next we will study diastolic function during tamponade in a similar group of conscious dogs. When compared to tamponade under control conditions in tamponade during beta blockade the cardiac output response is the same, stroke volume is greater, and heart rate is constant. We will study the cardiac output response to control tamponade, tamponade during beta blockade, and tamponade during beta blockage with heart rate adjusted to equal that during control tamponade at each intrapericardial pressure. Comparison of the cardiac output achieved at each intrapericardial pressure in these three states will allow us to determine the relative importance of myocardial contractility, left ventricular filling time, and filling rate on cardiac output during cardiac tamponade and test the hypothesis that left ventricular filling time is more important than inotropic state in maintaining cardiac output during tamponade. Further, since our model quantitates left ventricular filling without altering left atrial or mitral annular function, these data can be used to test the hypothesis that when intrapericardial pressure exceeds ventricular filling pressures during tamponade the left atrium acts as a Starling resistor severely restricting cardiac filling and making it more sensitive to the effects of respiration and increasing heart rate and preventing diastolic suction or septal shifting from influencing the left ventricular filling rate.